Histological analysis of normal avian and mammalian otic development suggests a complex interaction between the columellar (stapedial) and capsular chondrocytes in annular ligament formation. Similarity in columellar defects, notably footplate absence or fixation, seen in explanted avian otic rudiments and in drug-treated embryos, suggests mechanical factors may be involved in this interaction. High mortalities, and extreme cranio-facial defects seen in avian embryos treated with teratogens during neural crest cell migration and poliferation, suggest that primary genetic lesions of these cells would be lethal, so that only secondary growth phenomena are responsible for otic and cranio-facial defects. Comparable studies are planned with mouse embryos: results will be compared with mutant mouse otic morphogenesis. Experiments on avian tympanic wound healing are resolving some of the contradictions reported in mammalian studies. While complete closure occurs, considerable mesenchymal hyperplasia continues for some time, probably associated with remodeling of the extra-cellular fibrillar components. Neither middle ear infection, nor squamous epithelial metaplasia have been observed. These studies are to be extended to mammalian models.